Jackson, Miss., is the most obese city in the United States for 2017, according to the personal finance website WalletHub.

The city topped the ranking of the 100 heaviest metro areas in the country with a score of 84.9 out of a possible 100 points based on 17 key metrics in three broad categories: obese and overweight people (50 points), weight-related health problems (30 points), and health environment (20 points), according to WalletHub.

[email protected]

Jackson, Miss., is the most obese city in the United States for 2017, according to the personal finance website WalletHub.

The city topped the ranking of the 100 heaviest metro areas in the country with a score of 84.9 out of a possible 100 points based on 17 key metrics in three broad categories: obese and overweight people (50 points), weight-related health problems (30 points), and health environment (20 points), according to WalletHub.

[email protected]

Jackson, Miss., is the most obese city in the United States for 2017, according to the personal finance website WalletHub.

The city topped the ranking of the 100 heaviest metro areas in the country with a score of 84.9 out of a possible 100 points based on 17 key metrics in three broad categories: obese and overweight people (50 points), weight-related health problems (30 points), and health environment (20 points), according to WalletHub.

[email protected]

With the March 24 demise of the American Health Care Act, Republican leaders in Congress and in the White House have said that the Affordable Care Act will remain in place for the foreseeable future. While the ACA has brought about a number of health reforms that benefit physicians and their patients, other provisions have increased physician hassle and headache.

[polldaddy:9708248]

Check back soon to see if your colleagues agree on what part of the ACA should be changed, or email me your thoughts on the business of medicine.

[email protected]

On Twitter @denisefulton

With the March 24 demise of the American Health Care Act, Republican leaders in Congress and in the White House have said that the Affordable Care Act will remain in place for the foreseeable future. While the ACA has brought about a number of health reforms that benefit physicians and their patients, other provisions have increased physician hassle and headache.

[polldaddy:9708248]

Check back soon to see if your colleagues agree on what part of the ACA should be changed, or email me your thoughts on the business of medicine.

[email protected]

On Twitter @denisefulton

With the March 24 demise of the American Health Care Act, Republican leaders in Congress and in the White House have said that the Affordable Care Act will remain in place for the foreseeable future. While the ACA has brought about a number of health reforms that benefit physicians and their patients, other provisions have increased physician hassle and headache.

[polldaddy:9708248]

Check back soon to see if your colleagues agree on what part of the ACA should be changed, or email me your thoughts on the business of medicine.

[email protected]

On Twitter @denisefulton

HOUSTON—Cardiovascular risk factors in middle age may increase the risk of dementia in later years, according to a subanalysis of a 25-year atherosclerosis study.

Other conditions that significantly increased the likelihood of late-life dementia were hypertension and smoking, both of which augmented the risk by 40%.

Dr. Gottesman’s subanalysis of the biracial Atherosclerosis Risk in Communities-Neurocognitive Study (ARIC-NCS) also identified racial differences in dementia risk. Smoking was a risk factor for dementia in whites, but not in blacks. In addition, although the results were not significantly different by race, diabetes appeared to increase the risk more among blacks than whites, and hypertension increased the risk of dementia more among whites than blacks.

Analyzing Data From a Study of Atherosclerosis

The ARIC study, sponsored by the National Heart, Lung, and Blood Institute, is a prospective epidemiologic study conducted in four US communities. ARIC is designed to investigate the causes and clinical outcomes of atherosclerosis, and variation in cardiovascular risk factors, medical care, and disease by race, gender, location, and date. The ARIC project has led to the publication of more than 1,700 articles in peer-reviewed journals to date.

A total of 15,792 participants have received an extensive examination, including medical, social, and demographic data. The first screen occurred between 1987 and 1989, and participants were reexamined every three years through 1998, and then again 15 years later. Follow-up occurs yearly by telephone to maintain contact with participants and to assess the health status of the cohort.

The ARIC-NCS study includes about 10,000 of the ARIC participants. Of these patients, 6,471 completed the fifth visit, which occurred during 2011–2013. The participants have undergone cognitive and neurologic assessments to diagnose mild cognitive impairment or dementia and assign an etiology for any cognitive disorder; some also have undergone brain imaging. Last year, investigators published preliminary findings from the study, including that approximately 30% of participants had received a diagnosis of dementia or mild cognitive impairment.

Dr. Gottesman sought to determine the extent to which these subjects’ baseline cardiovascular risk factors influenced their risk of cognitive decline or dementia. She assessed risk for the entire cohort, and then assessed the risk for black and white subjects separately.

Genetic Status Had Largest Effect

In all, 1,516 participants (23%) developed dementia. In the total cohort, dementia was significantly associated with increasing age. Subjects between ages 50 and 54 when first examined had twice the risk of dementia during follow-up, compared with younger subjects, while those between ages 60 and 66 had eight times greater risk. Black race conferred an increased risk, compared with white race (hazard ratio [HR], 1.3). Education of less than a high school degree was associated with a 40% increased risk of dementia. Having at least one copy of the APOE4 allele doubled the risk of dementia.

Increasing BMI did not increase the risk of dementia, Dr. Gottesman noted. Smoking, however, increased the risk of dementia by 40%, as did prehypertension and hypertension. Dyslipidemia was not associated with any increased risk. Diabetes increased the risk of dementia by 80%.

Dr. Gottesman found significant differences in the way the factors affected risk in white and black subjects. Age exerted a greater influence on dementia risk in whites than it did in blacks. The risk was approximately doubled in both groups for people between ages 50 and 54 at baseline. But for patients between ages 55 and 59 at baseline, dementia risk was significantly higher in whites than in blacks (HR, 4.4 vs 3.5). The risk differential was even greater between whites and blacks who were between ages 60 and 66 (HR, 9.5 vs 6.2).

Blacks with low education had a greater risk of dementia than did whites (HR, 1.6 vs 1.3). APOE4 status (ie, having at least one allele) more than doubled the risk of dementia for whites (HR, 2.2), but had a weaker effect in blacks (HR, 1.6).

Obesity increased the risk of dementia by 22% for whites, but it had no influence on risk among blacks. Current smoking increased the risk for whites by 62%, but was not a significant risk factor for blacks. Prehypertension also had a greater effect among whites, increasing the risk by 35%, compared with a nonsignificant 17% increase for blacks, but the difference was not statistically significant. Hypertension increased the risk of dementia similarly in both groups (37% and 36%, respectively). Diabetes increased the risk of dementia more in blacks than it did in whites (85% vs 69%), but the racial difference was not statistically significant.

“We do not have a clear explanation of these disparities in dementia risk with regard to race,” said Dr. Gottesman. “It could be, though, that even if a risk factor has the same relationship with dementia in both groups, if it is more prevalent in one group, that may somewhat account for this larger population-attributable risk.”

—Michelle G. Sullivan

Suggested Reading

Baumgart M, Snyder HM, Carrillo MC, et al. Summary of the evidence on modifiable risk factors for cognitive decline and dementia: A population-based perspective. Alzheimers Dement. 2015;11(6):718-726.

Exalto LG, Quesenberry CP, Barnes D, et al. Midlife risk score for the prediction of dementia four decades later. Alzheimers Dement. 2014;10(5):562-570.

Hessler JB, Ander KH, Brönner M, et al. Predicting dementia in primary care patients with a cardiovascular health metric: a prospective population-based study. BMC Neurol. 2016;16:116.

Knopman DS, Gottesman RF, Sharrett AR, et al. Mild cognitive impairment and dementia prevalence: The Atherosclerosis Risk in Communities Neurocognitive Study (ARIC-NCS). Alzheimers Dement (Amst). 2016;2:1-11.

Virta JJ, Heikkilä K, Perola M, et al. Midlife cardiovascular risk factors and late cognitive impairment. Eur J Epidemiol. 2013;28(5):405-416.

HOUSTON—Cardiovascular risk factors in middle age may increase the risk of dementia in later years, according to a subanalysis of a 25-year atherosclerosis study.

Other conditions that significantly increased the likelihood of late-life dementia were hypertension and smoking, both of which augmented the risk by 40%.

Dr. Gottesman’s subanalysis of the biracial Atherosclerosis Risk in Communities-Neurocognitive Study (ARIC-NCS) also identified racial differences in dementia risk. Smoking was a risk factor for dementia in whites, but not in blacks. In addition, although the results were not significantly different by race, diabetes appeared to increase the risk more among blacks than whites, and hypertension increased the risk of dementia more among whites than blacks.

Analyzing Data From a Study of Atherosclerosis

The ARIC study, sponsored by the National Heart, Lung, and Blood Institute, is a prospective epidemiologic study conducted in four US communities. ARIC is designed to investigate the causes and clinical outcomes of atherosclerosis, and variation in cardiovascular risk factors, medical care, and disease by race, gender, location, and date. The ARIC project has led to the publication of more than 1,700 articles in peer-reviewed journals to date.

A total of 15,792 participants have received an extensive examination, including medical, social, and demographic data. The first screen occurred between 1987 and 1989, and participants were reexamined every three years through 1998, and then again 15 years later. Follow-up occurs yearly by telephone to maintain contact with participants and to assess the health status of the cohort.

The ARIC-NCS study includes about 10,000 of the ARIC participants. Of these patients, 6,471 completed the fifth visit, which occurred during 2011–2013. The participants have undergone cognitive and neurologic assessments to diagnose mild cognitive impairment or dementia and assign an etiology for any cognitive disorder; some also have undergone brain imaging. Last year, investigators published preliminary findings from the study, including that approximately 30% of participants had received a diagnosis of dementia or mild cognitive impairment.

Dr. Gottesman sought to determine the extent to which these subjects’ baseline cardiovascular risk factors influenced their risk of cognitive decline or dementia. She assessed risk for the entire cohort, and then assessed the risk for black and white subjects separately.

Genetic Status Had Largest Effect

In all, 1,516 participants (23%) developed dementia. In the total cohort, dementia was significantly associated with increasing age. Subjects between ages 50 and 54 when first examined had twice the risk of dementia during follow-up, compared with younger subjects, while those between ages 60 and 66 had eight times greater risk. Black race conferred an increased risk, compared with white race (hazard ratio [HR], 1.3). Education of less than a high school degree was associated with a 40% increased risk of dementia. Having at least one copy of the APOE4 allele doubled the risk of dementia.

Increasing BMI did not increase the risk of dementia, Dr. Gottesman noted. Smoking, however, increased the risk of dementia by 40%, as did prehypertension and hypertension. Dyslipidemia was not associated with any increased risk. Diabetes increased the risk of dementia by 80%.

Dr. Gottesman found significant differences in the way the factors affected risk in white and black subjects. Age exerted a greater influence on dementia risk in whites than it did in blacks. The risk was approximately doubled in both groups for people between ages 50 and 54 at baseline. But for patients between ages 55 and 59 at baseline, dementia risk was significantly higher in whites than in blacks (HR, 4.4 vs 3.5). The risk differential was even greater between whites and blacks who were between ages 60 and 66 (HR, 9.5 vs 6.2).

Blacks with low education had a greater risk of dementia than did whites (HR, 1.6 vs 1.3). APOE4 status (ie, having at least one allele) more than doubled the risk of dementia for whites (HR, 2.2), but had a weaker effect in blacks (HR, 1.6).

Obesity increased the risk of dementia by 22% for whites, but it had no influence on risk among blacks. Current smoking increased the risk for whites by 62%, but was not a significant risk factor for blacks. Prehypertension also had a greater effect among whites, increasing the risk by 35%, compared with a nonsignificant 17% increase for blacks, but the difference was not statistically significant. Hypertension increased the risk of dementia similarly in both groups (37% and 36%, respectively). Diabetes increased the risk of dementia more in blacks than it did in whites (85% vs 69%), but the racial difference was not statistically significant.

“We do not have a clear explanation of these disparities in dementia risk with regard to race,” said Dr. Gottesman. “It could be, though, that even if a risk factor has the same relationship with dementia in both groups, if it is more prevalent in one group, that may somewhat account for this larger population-attributable risk.”

—Michelle G. Sullivan

Suggested Reading

Baumgart M, Snyder HM, Carrillo MC, et al. Summary of the evidence on modifiable risk factors for cognitive decline and dementia: A population-based perspective. Alzheimers Dement. 2015;11(6):718-726.

Exalto LG, Quesenberry CP, Barnes D, et al. Midlife risk score for the prediction of dementia four decades later. Alzheimers Dement. 2014;10(5):562-570.

Hessler JB, Ander KH, Brönner M, et al. Predicting dementia in primary care patients with a cardiovascular health metric: a prospective population-based study. BMC Neurol. 2016;16:116.

Knopman DS, Gottesman RF, Sharrett AR, et al. Mild cognitive impairment and dementia prevalence: The Atherosclerosis Risk in Communities Neurocognitive Study (ARIC-NCS). Alzheimers Dement (Amst). 2016;2:1-11.

Virta JJ, Heikkilä K, Perola M, et al. Midlife cardiovascular risk factors and late cognitive impairment. Eur J Epidemiol. 2013;28(5):405-416.

HOUSTON—Cardiovascular risk factors in middle age may increase the risk of dementia in later years, according to a subanalysis of a 25-year atherosclerosis study.

Other conditions that significantly increased the likelihood of late-life dementia were hypertension and smoking, both of which augmented the risk by 40%.

Dr. Gottesman’s subanalysis of the biracial Atherosclerosis Risk in Communities-Neurocognitive Study (ARIC-NCS) also identified racial differences in dementia risk. Smoking was a risk factor for dementia in whites, but not in blacks. In addition, although the results were not significantly different by race, diabetes appeared to increase the risk more among blacks than whites, and hypertension increased the risk of dementia more among whites than blacks.

Analyzing Data From a Study of Atherosclerosis

The ARIC study, sponsored by the National Heart, Lung, and Blood Institute, is a prospective epidemiologic study conducted in four US communities. ARIC is designed to investigate the causes and clinical outcomes of atherosclerosis, and variation in cardiovascular risk factors, medical care, and disease by race, gender, location, and date. The ARIC project has led to the publication of more than 1,700 articles in peer-reviewed journals to date.

A total of 15,792 participants have received an extensive examination, including medical, social, and demographic data. The first screen occurred between 1987 and 1989, and participants were reexamined every three years through 1998, and then again 15 years later. Follow-up occurs yearly by telephone to maintain contact with participants and to assess the health status of the cohort.

The ARIC-NCS study includes about 10,000 of the ARIC participants. Of these patients, 6,471 completed the fifth visit, which occurred during 2011–2013. The participants have undergone cognitive and neurologic assessments to diagnose mild cognitive impairment or dementia and assign an etiology for any cognitive disorder; some also have undergone brain imaging. Last year, investigators published preliminary findings from the study, including that approximately 30% of participants had received a diagnosis of dementia or mild cognitive impairment.

Dr. Gottesman sought to determine the extent to which these subjects’ baseline cardiovascular risk factors influenced their risk of cognitive decline or dementia. She assessed risk for the entire cohort, and then assessed the risk for black and white subjects separately.

Genetic Status Had Largest Effect

In all, 1,516 participants (23%) developed dementia. In the total cohort, dementia was significantly associated with increasing age. Subjects between ages 50 and 54 when first examined had twice the risk of dementia during follow-up, compared with younger subjects, while those between ages 60 and 66 had eight times greater risk. Black race conferred an increased risk, compared with white race (hazard ratio [HR], 1.3). Education of less than a high school degree was associated with a 40% increased risk of dementia. Having at least one copy of the APOE4 allele doubled the risk of dementia.

Increasing BMI did not increase the risk of dementia, Dr. Gottesman noted. Smoking, however, increased the risk of dementia by 40%, as did prehypertension and hypertension. Dyslipidemia was not associated with any increased risk. Diabetes increased the risk of dementia by 80%.

Dr. Gottesman found significant differences in the way the factors affected risk in white and black subjects. Age exerted a greater influence on dementia risk in whites than it did in blacks. The risk was approximately doubled in both groups for people between ages 50 and 54 at baseline. But for patients between ages 55 and 59 at baseline, dementia risk was significantly higher in whites than in blacks (HR, 4.4 vs 3.5). The risk differential was even greater between whites and blacks who were between ages 60 and 66 (HR, 9.5 vs 6.2).

Blacks with low education had a greater risk of dementia than did whites (HR, 1.6 vs 1.3). APOE4 status (ie, having at least one allele) more than doubled the risk of dementia for whites (HR, 2.2), but had a weaker effect in blacks (HR, 1.6).

Obesity increased the risk of dementia by 22% for whites, but it had no influence on risk among blacks. Current smoking increased the risk for whites by 62%, but was not a significant risk factor for blacks. Prehypertension also had a greater effect among whites, increasing the risk by 35%, compared with a nonsignificant 17% increase for blacks, but the difference was not statistically significant. Hypertension increased the risk of dementia similarly in both groups (37% and 36%, respectively). Diabetes increased the risk of dementia more in blacks than it did in whites (85% vs 69%), but the racial difference was not statistically significant.

“We do not have a clear explanation of these disparities in dementia risk with regard to race,” said Dr. Gottesman. “It could be, though, that even if a risk factor has the same relationship with dementia in both groups, if it is more prevalent in one group, that may somewhat account for this larger population-attributable risk.”

—Michelle G. Sullivan

Suggested Reading

Baumgart M, Snyder HM, Carrillo MC, et al. Summary of the evidence on modifiable risk factors for cognitive decline and dementia: A population-based perspective. Alzheimers Dement. 2015;11(6):718-726.

Exalto LG, Quesenberry CP, Barnes D, et al. Midlife risk score for the prediction of dementia four decades later. Alzheimers Dement. 2014;10(5):562-570.

Hessler JB, Ander KH, Brönner M, et al. Predicting dementia in primary care patients with a cardiovascular health metric: a prospective population-based study. BMC Neurol. 2016;16:116.

Knopman DS, Gottesman RF, Sharrett AR, et al. Mild cognitive impairment and dementia prevalence: The Atherosclerosis Risk in Communities Neurocognitive Study (ARIC-NCS). Alzheimers Dement (Amst). 2016;2:1-11.

Virta JJ, Heikkilä K, Perola M, et al. Midlife cardiovascular risk factors and late cognitive impairment. Eur J Epidemiol. 2013;28(5):405-416.

All patients with chronic insomnia should receive cognitive behavioral therapy as a primary intervention, and clinicians should use a shared decision-making approach when determining whether patients should start pharmacotherapy, according to a new guideline developed by the American Academy of Sleep Medicine (AASM). The guideline, which includes 14 recommendations, was published in the February 15 issue of the Journal of Clinical Sleep Medicine. It is the first guideline from the AASM to provide comprehensive evidence-based analyses of individual drugs commonly used to treat chronic insomnia disorder.

Chronic insomnia is associated with increased work absenteeism and impairment in functional status. Studies have also identified persistent insomnia as a significant risk factor for the development of psychiatric disorders, especially mood disorder. Pharmacologic treatment of insomnia is the most widely used approach to therapy, after treatment of comorbidities. No evidence-based clinical guideline had been published previously, however. The AASM commissioned a task force of four sleep medicine experts to develop the clinical guideline for treatment of chronic insomnia in adults.

The task force conducted a systematic review to identify randomized controlled trials. In addition, the group used the Grading of Recommendations Assessment, Development, and Evaluation process to assess the evidence. Recommendations were then made based on the quality of evidence, the balance of benefits and harms, and patient values and preferences.

Sleep Onset Insomnia Treatment Recommendations

The guideline recommends eszopiclone for the treatment of sleep onset insomnia, based on trials of 2-mg and 3-mg doses of the drug. Mean reduction of sleep latency was 14 minutes greater with eszopiclone than with placebo. Researchers also observed a moderate-to-large improvement in quality of sleep when they compared eszopiclone with placebo.

The experts also recommend ramelteon, based on trials of 8-mg doses of the drug. Mean reduction of sleep latency was nine minutes greater with ramelteon than with placebo. Ramelteon may not improve quality of sleep, however. Clinicians also are advised to use temazepam, based on trials of 15-mg doses. Temazepam reduced sleep latency by 37 minutes, compared with placebo, and provided a small improvement in quality of sleep.

The quality of evidence for the use of triazolam was high, and the drug reduced sleep latency by nine minutes, compared with placebo. The task force determined that the majority of patients would be more likely to use triazolam, compared with no treatment, but many would not use it. Zaleplon was recommended based on trials of 5-mg and 10-mg doses. It reduced sleep latency by 10 minutes, compared with placebo. Finally, zolpidem reduced sleep latency by five to 12 minutes, compared with placebo, and was associated with a moderate improvement in quality of sleep. The quality of evidence was very low, however.

Sleep Maintenance Insomnia Recommendations

The task force found four studies evaluating a 3-mg dose of doxepin and four studies investigating a 6-mg dose in sleep maintenance insomnia. Mean improvement in total sleep time with the drug was 26–32 min longer, compared with placebo. The mean reduction in wake after sleep onset (WASO) associated with doxepin was 22–23 min greater, compared with placebo.

The recommendation for the use of eszopiclone was based on trials of 2-mg and 3-mg doses of the drug. Mean improvement in total sleep time was 28–57 min longer with eszopiclone, compared with placebo. Mean reduction in WASO was 10–14 min greater with eszopiclone, compared with placebo.

Trials of 15-mg doses of temazepam were the basis for the task force’s recommendation of the drug. Mean improvement in total sleep time with temazepam was 99 min longer, compared with placebo. The drug’s effect on WASO was not reported. Compared with placebo, temazepam may provide a small improvement in quality of sleep.

Suvorexant was evaluated in trials of 10-mg, 15–20-mg, and 20-mg doses. Mean improvement in total sleep time was 10 min longer with suvorexant, compared with placebo. Mean reduction in WASO was 16–28 min greater with suvorexant, compared to placebo.

The guideline also recommends zolpidem, based on trials of 10-mg doses. Zolpidem provided a mean improvement in total sleep time that was 29 min longer, compared with placebo. The mean reduction in WASO was 25 min greater with zolpidem, compared with placebo.

Certain Drugs Are Not Recommended

Several drugs were not recommended for treating sleep onset or sleep maintenance insomnia. The task force suggests that clinicians not use diphenhydramine, because the evidence suggests that it is not effective for improving sleep onset or total sleep time. Similarly, evidence suggests that the effects of tiagabine on objective and subjective measures of sleep latency are clinically insignificant, and the drug’s harms may outweigh its benefits. Sleep outcome variables also did not improve with trazodone to a clinically significant degree. The task force also suggested that clinicians not use melatonin, valerian, or L-tryptophan because of the treatments’ lack of clinically significant effects.

All recommendations were classified as weak, due to the task force’s low degree of certainty in the appropriateness of the patient-care strategy. Further study is required to determine the drugs’ efficacy or lack thereof, said the task force. “Clinicians must continue to exercise sound clinical judgment based not only on these recommendations, but also on clinical experience, prior patient response, patient preferences, and potential adverse effects,” the authors concluded.

—Erica Tricarico

Suggested Reading

Sateia MJ, Buysse DJ, Krystal AD, et al. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: An American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(2):307-349.

All patients with chronic insomnia should receive cognitive behavioral therapy as a primary intervention, and clinicians should use a shared decision-making approach when determining whether patients should start pharmacotherapy, according to a new guideline developed by the American Academy of Sleep Medicine (AASM). The guideline, which includes 14 recommendations, was published in the February 15 issue of the Journal of Clinical Sleep Medicine. It is the first guideline from the AASM to provide comprehensive evidence-based analyses of individual drugs commonly used to treat chronic insomnia disorder.

Chronic insomnia is associated with increased work absenteeism and impairment in functional status. Studies have also identified persistent insomnia as a significant risk factor for the development of psychiatric disorders, especially mood disorder. Pharmacologic treatment of insomnia is the most widely used approach to therapy, after treatment of comorbidities. No evidence-based clinical guideline had been published previously, however. The AASM commissioned a task force of four sleep medicine experts to develop the clinical guideline for treatment of chronic insomnia in adults.

The task force conducted a systematic review to identify randomized controlled trials. In addition, the group used the Grading of Recommendations Assessment, Development, and Evaluation process to assess the evidence. Recommendations were then made based on the quality of evidence, the balance of benefits and harms, and patient values and preferences.

Sleep Onset Insomnia Treatment Recommendations

The guideline recommends eszopiclone for the treatment of sleep onset insomnia, based on trials of 2-mg and 3-mg doses of the drug. Mean reduction of sleep latency was 14 minutes greater with eszopiclone than with placebo. Researchers also observed a moderate-to-large improvement in quality of sleep when they compared eszopiclone with placebo.

The experts also recommend ramelteon, based on trials of 8-mg doses of the drug. Mean reduction of sleep latency was nine minutes greater with ramelteon than with placebo. Ramelteon may not improve quality of sleep, however. Clinicians also are advised to use temazepam, based on trials of 15-mg doses. Temazepam reduced sleep latency by 37 minutes, compared with placebo, and provided a small improvement in quality of sleep.

The quality of evidence for the use of triazolam was high, and the drug reduced sleep latency by nine minutes, compared with placebo. The task force determined that the majority of patients would be more likely to use triazolam, compared with no treatment, but many would not use it. Zaleplon was recommended based on trials of 5-mg and 10-mg doses. It reduced sleep latency by 10 minutes, compared with placebo. Finally, zolpidem reduced sleep latency by five to 12 minutes, compared with placebo, and was associated with a moderate improvement in quality of sleep. The quality of evidence was very low, however.

Sleep Maintenance Insomnia Recommendations

The task force found four studies evaluating a 3-mg dose of doxepin and four studies investigating a 6-mg dose in sleep maintenance insomnia. Mean improvement in total sleep time with the drug was 26–32 min longer, compared with placebo. The mean reduction in wake after sleep onset (WASO) associated with doxepin was 22–23 min greater, compared with placebo.

The recommendation for the use of eszopiclone was based on trials of 2-mg and 3-mg doses of the drug. Mean improvement in total sleep time was 28–57 min longer with eszopiclone, compared with placebo. Mean reduction in WASO was 10–14 min greater with eszopiclone, compared with placebo.

Trials of 15-mg doses of temazepam were the basis for the task force’s recommendation of the drug. Mean improvement in total sleep time with temazepam was 99 min longer, compared with placebo. The drug’s effect on WASO was not reported. Compared with placebo, temazepam may provide a small improvement in quality of sleep.

Suvorexant was evaluated in trials of 10-mg, 15–20-mg, and 20-mg doses. Mean improvement in total sleep time was 10 min longer with suvorexant, compared with placebo. Mean reduction in WASO was 16–28 min greater with suvorexant, compared to placebo.

The guideline also recommends zolpidem, based on trials of 10-mg doses. Zolpidem provided a mean improvement in total sleep time that was 29 min longer, compared with placebo. The mean reduction in WASO was 25 min greater with zolpidem, compared with placebo.

Certain Drugs Are Not Recommended

Several drugs were not recommended for treating sleep onset or sleep maintenance insomnia. The task force suggests that clinicians not use diphenhydramine, because the evidence suggests that it is not effective for improving sleep onset or total sleep time. Similarly, evidence suggests that the effects of tiagabine on objective and subjective measures of sleep latency are clinically insignificant, and the drug’s harms may outweigh its benefits. Sleep outcome variables also did not improve with trazodone to a clinically significant degree. The task force also suggested that clinicians not use melatonin, valerian, or L-tryptophan because of the treatments’ lack of clinically significant effects.

All recommendations were classified as weak, due to the task force’s low degree of certainty in the appropriateness of the patient-care strategy. Further study is required to determine the drugs’ efficacy or lack thereof, said the task force. “Clinicians must continue to exercise sound clinical judgment based not only on these recommendations, but also on clinical experience, prior patient response, patient preferences, and potential adverse effects,” the authors concluded.

—Erica Tricarico

Suggested Reading

Sateia MJ, Buysse DJ, Krystal AD, et al. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: An American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(2):307-349.

All patients with chronic insomnia should receive cognitive behavioral therapy as a primary intervention, and clinicians should use a shared decision-making approach when determining whether patients should start pharmacotherapy, according to a new guideline developed by the American Academy of Sleep Medicine (AASM). The guideline, which includes 14 recommendations, was published in the February 15 issue of the Journal of Clinical Sleep Medicine. It is the first guideline from the AASM to provide comprehensive evidence-based analyses of individual drugs commonly used to treat chronic insomnia disorder.

Chronic insomnia is associated with increased work absenteeism and impairment in functional status. Studies have also identified persistent insomnia as a significant risk factor for the development of psychiatric disorders, especially mood disorder. Pharmacologic treatment of insomnia is the most widely used approach to therapy, after treatment of comorbidities. No evidence-based clinical guideline had been published previously, however. The AASM commissioned a task force of four sleep medicine experts to develop the clinical guideline for treatment of chronic insomnia in adults.

The task force conducted a systematic review to identify randomized controlled trials. In addition, the group used the Grading of Recommendations Assessment, Development, and Evaluation process to assess the evidence. Recommendations were then made based on the quality of evidence, the balance of benefits and harms, and patient values and preferences.

Sleep Onset Insomnia Treatment Recommendations

The guideline recommends eszopiclone for the treatment of sleep onset insomnia, based on trials of 2-mg and 3-mg doses of the drug. Mean reduction of sleep latency was 14 minutes greater with eszopiclone than with placebo. Researchers also observed a moderate-to-large improvement in quality of sleep when they compared eszopiclone with placebo.

The experts also recommend ramelteon, based on trials of 8-mg doses of the drug. Mean reduction of sleep latency was nine minutes greater with ramelteon than with placebo. Ramelteon may not improve quality of sleep, however. Clinicians also are advised to use temazepam, based on trials of 15-mg doses. Temazepam reduced sleep latency by 37 minutes, compared with placebo, and provided a small improvement in quality of sleep.

The quality of evidence for the use of triazolam was high, and the drug reduced sleep latency by nine minutes, compared with placebo. The task force determined that the majority of patients would be more likely to use triazolam, compared with no treatment, but many would not use it. Zaleplon was recommended based on trials of 5-mg and 10-mg doses. It reduced sleep latency by 10 minutes, compared with placebo. Finally, zolpidem reduced sleep latency by five to 12 minutes, compared with placebo, and was associated with a moderate improvement in quality of sleep. The quality of evidence was very low, however.

Sleep Maintenance Insomnia Recommendations

The task force found four studies evaluating a 3-mg dose of doxepin and four studies investigating a 6-mg dose in sleep maintenance insomnia. Mean improvement in total sleep time with the drug was 26–32 min longer, compared with placebo. The mean reduction in wake after sleep onset (WASO) associated with doxepin was 22–23 min greater, compared with placebo.

The recommendation for the use of eszopiclone was based on trials of 2-mg and 3-mg doses of the drug. Mean improvement in total sleep time was 28–57 min longer with eszopiclone, compared with placebo. Mean reduction in WASO was 10–14 min greater with eszopiclone, compared with placebo.

Trials of 15-mg doses of temazepam were the basis for the task force’s recommendation of the drug. Mean improvement in total sleep time with temazepam was 99 min longer, compared with placebo. The drug’s effect on WASO was not reported. Compared with placebo, temazepam may provide a small improvement in quality of sleep.

Suvorexant was evaluated in trials of 10-mg, 15–20-mg, and 20-mg doses. Mean improvement in total sleep time was 10 min longer with suvorexant, compared with placebo. Mean reduction in WASO was 16–28 min greater with suvorexant, compared to placebo.

The guideline also recommends zolpidem, based on trials of 10-mg doses. Zolpidem provided a mean improvement in total sleep time that was 29 min longer, compared with placebo. The mean reduction in WASO was 25 min greater with zolpidem, compared with placebo.

Certain Drugs Are Not Recommended

Several drugs were not recommended for treating sleep onset or sleep maintenance insomnia. The task force suggests that clinicians not use diphenhydramine, because the evidence suggests that it is not effective for improving sleep onset or total sleep time. Similarly, evidence suggests that the effects of tiagabine on objective and subjective measures of sleep latency are clinically insignificant, and the drug’s harms may outweigh its benefits. Sleep outcome variables also did not improve with trazodone to a clinically significant degree. The task force also suggested that clinicians not use melatonin, valerian, or L-tryptophan because of the treatments’ lack of clinically significant effects.

All recommendations were classified as weak, due to the task force’s low degree of certainty in the appropriateness of the patient-care strategy. Further study is required to determine the drugs’ efficacy or lack thereof, said the task force. “Clinicians must continue to exercise sound clinical judgment based not only on these recommendations, but also on clinical experience, prior patient response, patient preferences, and potential adverse effects,” the authors concluded.

—Erica Tricarico

Suggested Reading

Sateia MJ, Buysse DJ, Krystal AD, et al. Clinical practice guideline for the pharmacologic treatment of chronic insomnia in adults: An American Academy of Sleep Medicine clinical practice guideline. J Clin Sleep Med. 2017;13(2):307-349.

ATLANTA – By the time adults with severe, chronic ear pain end up at the Mayo Clinic in Rochester, Minn., it’s not uncommon for them to have failed antibiotics and gone through a dozen or more sets of ear tubes that didn’t work, followed by surgery – mastoidectomy – to no avail.

“When they get to us, they are struggling. It’s miserable,” said allergist Erin Willits, MD, of Mayo’s division of allergy and immunology inRochester, Minn.

[email protected]

ATLANTA – By the time adults with severe, chronic ear pain end up at the Mayo Clinic in Rochester, Minn., it’s not uncommon for them to have failed antibiotics and gone through a dozen or more sets of ear tubes that didn’t work, followed by surgery – mastoidectomy – to no avail.

“When they get to us, they are struggling. It’s miserable,” said allergist Erin Willits, MD, of Mayo’s division of allergy and immunology inRochester, Minn.

[email protected]

ATLANTA – By the time adults with severe, chronic ear pain end up at the Mayo Clinic in Rochester, Minn., it’s not uncommon for them to have failed antibiotics and gone through a dozen or more sets of ear tubes that didn’t work, followed by surgery – mastoidectomy – to no avail.

“When they get to us, they are struggling. It’s miserable,” said allergist Erin Willits, MD, of Mayo’s division of allergy and immunology inRochester, Minn.

[email protected]

Intravenous magnesium does not benefit, and may harm, infants with moderate to severe acute bronchiolitis, investigators reported.

Compared with placebo, adding a single intravenous dose of magnesium sulfate (100 mg/kg) to usual care did not reduce time to medical readiness for discharge, even when patients had eczema or a family history of asthma, and was tied to more than a threefold rise in the rate of short-term readmissions, Khalid Al Ansari, MD, of Hamad Medical Corp. in Doha, Qatar, and his associates wrote in Chest. “To our knowledge, this is the first randomized study to investigate the effect of intravenous magnesium in a bronchiolitis population,” they added.

Bronchiolitis lacks new, inexpensive, readily available treatments, despite being a common reason for hospital admission, the researchers noted. For older children with moderate to severe exacerbations of asthma, a meta-analysis found that the addition of magnesium to usual care appeared to cut readmissions and shorten lengths of stay, compared with placebo. To explore magnesium therapy in younger children, the investigators enrolled 162 previously healthy infants up to 18 months old who had been admitted to the short-stay unit of a pediatric emergency center with a diagnosis of moderate to severe viral bronchiolitis. Patients received usual care with oral dexamethasone and nebulized 5% hypertonic saline in 1 mL of 1:1000 epinephrine, plus an intravenous 60-minute infusion with a blinded syringe of either 0.9% saline placebo or magnesium sulfate (100 mg/kg) (Chest. 2017 Mar 9. doi: 10.1016/j.chest.2017.03.002).

The primary endpoint, time to medical readiness for discharge, did not statistically differ between groups, averaging 24.1 (95% confidence interval, 20.0-29.1) hours with magnesium and 25.3 (95% CI, 20.3-31.5) hours with placebo (P = .91). Among patients with a history of eczema or a family history of asthma, mean times to readiness for discharge resembled those for the entire cohort and did not statistically differ based on treatment. Average Wang bronchiolitis severity scores also were similar between groups, as were rates of outpatient clinic visits (33.8% with magnesium and 27.2% with placebo). Thus, the trial identified “no benefit in adding intravenous magnesium for infant bronchiolitis, even in patients characterized to be at a higher risk for asthma,” the researchers concluded.

Strikingly, 2-week readmission rates were 19.5% with magnesium (95% CI, 11.3-30.1) and 6.2% with placebo (95% CI, 0.02-13.8; P = .016). Among patients with eczema or a family history of asthma, 2-week readmission rates also were significantly higher with magnesium (26.3%; 95% CI, 13.4-43.1) than with placebo (7.5%; 95% CI, 1.6-20.4; P = .034) These might have been chance findings, or magnesium might have masked worse bronchiolitis, prolonged the disease course, or interacted with 5% hypertonic saline or systemic corticosteroids, the investigators said. Intravenous magnesium might contribute to secondary relapse, especially among patients with eczema or a family history of asthma, they added.

Patients in this study had a median age of 3.7 months (range, 22 days to 17.6 months), about half had eczema or a family history of asthma, and 86% had positive nasopharyngeal virus swabs. Cardiopulmonary monitoring revealed no acute events during treatment. Of 16 readmissions in the magnesium group, 11 entered the infirmary and 4 entered the hospital. The five placebo readmissions included four to the infirmary and one to the hospital.

“As with other ‘negative studies,’ we may have failed to identify a benefit from intravenous magnesium in a patient subgroup because of our limited sample size,” the investigators wrote. “But we think our findings are generalizable to a similarly heterogeneous group of patients presenting for bronchiolitis care in a busy urban emergency department.”

Hamad Medical Corp. sponsored the study. The investigators reported having no conflicts of interest.

Intravenous magnesium does not benefit, and may harm, infants with moderate to severe acute bronchiolitis, investigators reported.

Compared with placebo, adding a single intravenous dose of magnesium sulfate (100 mg/kg) to usual care did not reduce time to medical readiness for discharge, even when patients had eczema or a family history of asthma, and was tied to more than a threefold rise in the rate of short-term readmissions, Khalid Al Ansari, MD, of Hamad Medical Corp. in Doha, Qatar, and his associates wrote in Chest. “To our knowledge, this is the first randomized study to investigate the effect of intravenous magnesium in a bronchiolitis population,” they added.

Bronchiolitis lacks new, inexpensive, readily available treatments, despite being a common reason for hospital admission, the researchers noted. For older children with moderate to severe exacerbations of asthma, a meta-analysis found that the addition of magnesium to usual care appeared to cut readmissions and shorten lengths of stay, compared with placebo. To explore magnesium therapy in younger children, the investigators enrolled 162 previously healthy infants up to 18 months old who had been admitted to the short-stay unit of a pediatric emergency center with a diagnosis of moderate to severe viral bronchiolitis. Patients received usual care with oral dexamethasone and nebulized 5% hypertonic saline in 1 mL of 1:1000 epinephrine, plus an intravenous 60-minute infusion with a blinded syringe of either 0.9% saline placebo or magnesium sulfate (100 mg/kg) (Chest. 2017 Mar 9. doi: 10.1016/j.chest.2017.03.002).

The primary endpoint, time to medical readiness for discharge, did not statistically differ between groups, averaging 24.1 (95% confidence interval, 20.0-29.1) hours with magnesium and 25.3 (95% CI, 20.3-31.5) hours with placebo (P = .91). Among patients with a history of eczema or a family history of asthma, mean times to readiness for discharge resembled those for the entire cohort and did not statistically differ based on treatment. Average Wang bronchiolitis severity scores also were similar between groups, as were rates of outpatient clinic visits (33.8% with magnesium and 27.2% with placebo). Thus, the trial identified “no benefit in adding intravenous magnesium for infant bronchiolitis, even in patients characterized to be at a higher risk for asthma,” the researchers concluded.

Strikingly, 2-week readmission rates were 19.5% with magnesium (95% CI, 11.3-30.1) and 6.2% with placebo (95% CI, 0.02-13.8; P = .016). Among patients with eczema or a family history of asthma, 2-week readmission rates also were significantly higher with magnesium (26.3%; 95% CI, 13.4-43.1) than with placebo (7.5%; 95% CI, 1.6-20.4; P = .034) These might have been chance findings, or magnesium might have masked worse bronchiolitis, prolonged the disease course, or interacted with 5% hypertonic saline or systemic corticosteroids, the investigators said. Intravenous magnesium might contribute to secondary relapse, especially among patients with eczema or a family history of asthma, they added.

Patients in this study had a median age of 3.7 months (range, 22 days to 17.6 months), about half had eczema or a family history of asthma, and 86% had positive nasopharyngeal virus swabs. Cardiopulmonary monitoring revealed no acute events during treatment. Of 16 readmissions in the magnesium group, 11 entered the infirmary and 4 entered the hospital. The five placebo readmissions included four to the infirmary and one to the hospital.

“As with other ‘negative studies,’ we may have failed to identify a benefit from intravenous magnesium in a patient subgroup because of our limited sample size,” the investigators wrote. “But we think our findings are generalizable to a similarly heterogeneous group of patients presenting for bronchiolitis care in a busy urban emergency department.”

Hamad Medical Corp. sponsored the study. The investigators reported having no conflicts of interest.

Intravenous magnesium does not benefit, and may harm, infants with moderate to severe acute bronchiolitis, investigators reported.

Compared with placebo, adding a single intravenous dose of magnesium sulfate (100 mg/kg) to usual care did not reduce time to medical readiness for discharge, even when patients had eczema or a family history of asthma, and was tied to more than a threefold rise in the rate of short-term readmissions, Khalid Al Ansari, MD, of Hamad Medical Corp. in Doha, Qatar, and his associates wrote in Chest. “To our knowledge, this is the first randomized study to investigate the effect of intravenous magnesium in a bronchiolitis population,” they added.

Bronchiolitis lacks new, inexpensive, readily available treatments, despite being a common reason for hospital admission, the researchers noted. For older children with moderate to severe exacerbations of asthma, a meta-analysis found that the addition of magnesium to usual care appeared to cut readmissions and shorten lengths of stay, compared with placebo. To explore magnesium therapy in younger children, the investigators enrolled 162 previously healthy infants up to 18 months old who had been admitted to the short-stay unit of a pediatric emergency center with a diagnosis of moderate to severe viral bronchiolitis. Patients received usual care with oral dexamethasone and nebulized 5% hypertonic saline in 1 mL of 1:1000 epinephrine, plus an intravenous 60-minute infusion with a blinded syringe of either 0.9% saline placebo or magnesium sulfate (100 mg/kg) (Chest. 2017 Mar 9. doi: 10.1016/j.chest.2017.03.002).

The primary endpoint, time to medical readiness for discharge, did not statistically differ between groups, averaging 24.1 (95% confidence interval, 20.0-29.1) hours with magnesium and 25.3 (95% CI, 20.3-31.5) hours with placebo (P = .91). Among patients with a history of eczema or a family history of asthma, mean times to readiness for discharge resembled those for the entire cohort and did not statistically differ based on treatment. Average Wang bronchiolitis severity scores also were similar between groups, as were rates of outpatient clinic visits (33.8% with magnesium and 27.2% with placebo). Thus, the trial identified “no benefit in adding intravenous magnesium for infant bronchiolitis, even in patients characterized to be at a higher risk for asthma,” the researchers concluded.

Strikingly, 2-week readmission rates were 19.5% with magnesium (95% CI, 11.3-30.1) and 6.2% with placebo (95% CI, 0.02-13.8; P = .016). Among patients with eczema or a family history of asthma, 2-week readmission rates also were significantly higher with magnesium (26.3%; 95% CI, 13.4-43.1) than with placebo (7.5%; 95% CI, 1.6-20.4; P = .034) These might have been chance findings, or magnesium might have masked worse bronchiolitis, prolonged the disease course, or interacted with 5% hypertonic saline or systemic corticosteroids, the investigators said. Intravenous magnesium might contribute to secondary relapse, especially among patients with eczema or a family history of asthma, they added.

Patients in this study had a median age of 3.7 months (range, 22 days to 17.6 months), about half had eczema or a family history of asthma, and 86% had positive nasopharyngeal virus swabs. Cardiopulmonary monitoring revealed no acute events during treatment. Of 16 readmissions in the magnesium group, 11 entered the infirmary and 4 entered the hospital. The five placebo readmissions included four to the infirmary and one to the hospital.

“As with other ‘negative studies,’ we may have failed to identify a benefit from intravenous magnesium in a patient subgroup because of our limited sample size,” the investigators wrote. “But we think our findings are generalizable to a similarly heterogeneous group of patients presenting for bronchiolitis care in a busy urban emergency department.”

Hamad Medical Corp. sponsored the study. The investigators reported having no conflicts of interest.

MIAMI—Among patients with Parkinson’s disease–associated mild cognitive impairment (MCI), Montreal Cognitive Assessment (MoCA) subscores in visuospatial function, attention, language, and orientation are the most useful in predicting conversion to dementia, according to research presented at the First Pan American Parkinson’s Disease and Movement Disorders Congress. Melissa Mackenzie, of the Division of Neurology at the University of British Columbia in Vancouver, Canada, and colleagues conducted a study to evaluate which subscores on the cognitive assessment predict conversion to dementia in patients with Parkinson’s disease–associated MCI.

The investigators searched the Pacific Parkinson’s Research Centre Database to identify patients with a diagnosis of idiopathic Parkinson’s disease who completed an itemized MoCA in the MCI range (ie, they had a corrected total score between 21 and 27) and who completed at least one other MoCA at least one year later. Patients taking potentially cognitive enhancing medications were excluded.

The researchers included in their study 529 assessments from 164 patients. They separated patients into three groups based on their last MoCA score—those who developed dementia (33 patients), those who returned to normal cognition (48 patients), and those who maintained MoCA scores in the MCI range (83 patients). In a model that predicted future MoCA score categories with 78% accuracy, the most important subscores were visuospatial, attention, language, and orientation, “but, interestingly, not delayed recall,” Dr. Mackenzie and colleagues said.

“A prevailing theory of cognitive decline in Parkinson’s disease postulates that visuospatial ‘posterior-cortical’ impairments are due to Lewy body deposition, whereas frontal executive dysfunction reflects ‘on–off’ state,” the researchers said. “Interestingly, language scores and memory function in delayed recall were the items that improved the most” in patients who reverted from MCI to normal cognition. “Whether the best approach to assess risk of conversion to dementia is to focus exclusively on these MoCA sections, or alternatively, employing multiple tests that target these cognitive domains, remains to be seen,” the researchers concluded. Patients with Parkinson’s disease–associated MCI at any time “should likely be followed more closely for cognitive decline, as they seem to be at increased risk for developing dementia, even if there is interval maintenance of MCI or return to normal cognition.”

—Jake Remaly

MIAMI—Among patients with Parkinson’s disease–associated mild cognitive impairment (MCI), Montreal Cognitive Assessment (MoCA) subscores in visuospatial function, attention, language, and orientation are the most useful in predicting conversion to dementia, according to research presented at the First Pan American Parkinson’s Disease and Movement Disorders Congress. Melissa Mackenzie, of the Division of Neurology at the University of British Columbia in Vancouver, Canada, and colleagues conducted a study to evaluate which subscores on the cognitive assessment predict conversion to dementia in patients with Parkinson’s disease–associated MCI.

The investigators searched the Pacific Parkinson’s Research Centre Database to identify patients with a diagnosis of idiopathic Parkinson’s disease who completed an itemized MoCA in the MCI range (ie, they had a corrected total score between 21 and 27) and who completed at least one other MoCA at least one year later. Patients taking potentially cognitive enhancing medications were excluded.

The researchers included in their study 529 assessments from 164 patients. They separated patients into three groups based on their last MoCA score—those who developed dementia (33 patients), those who returned to normal cognition (48 patients), and those who maintained MoCA scores in the MCI range (83 patients). In a model that predicted future MoCA score categories with 78% accuracy, the most important subscores were visuospatial, attention, language, and orientation, “but, interestingly, not delayed recall,” Dr. Mackenzie and colleagues said.

“A prevailing theory of cognitive decline in Parkinson’s disease postulates that visuospatial ‘posterior-cortical’ impairments are due to Lewy body deposition, whereas frontal executive dysfunction reflects ‘on–off’ state,” the researchers said. “Interestingly, language scores and memory function in delayed recall were the items that improved the most” in patients who reverted from MCI to normal cognition. “Whether the best approach to assess risk of conversion to dementia is to focus exclusively on these MoCA sections, or alternatively, employing multiple tests that target these cognitive domains, remains to be seen,” the researchers concluded. Patients with Parkinson’s disease–associated MCI at any time “should likely be followed more closely for cognitive decline, as they seem to be at increased risk for developing dementia, even if there is interval maintenance of MCI or return to normal cognition.”

—Jake Remaly

MIAMI—Among patients with Parkinson’s disease–associated mild cognitive impairment (MCI), Montreal Cognitive Assessment (MoCA) subscores in visuospatial function, attention, language, and orientation are the most useful in predicting conversion to dementia, according to research presented at the First Pan American Parkinson’s Disease and Movement Disorders Congress. Melissa Mackenzie, of the Division of Neurology at the University of British Columbia in Vancouver, Canada, and colleagues conducted a study to evaluate which subscores on the cognitive assessment predict conversion to dementia in patients with Parkinson’s disease–associated MCI.

The investigators searched the Pacific Parkinson’s Research Centre Database to identify patients with a diagnosis of idiopathic Parkinson’s disease who completed an itemized MoCA in the MCI range (ie, they had a corrected total score between 21 and 27) and who completed at least one other MoCA at least one year later. Patients taking potentially cognitive enhancing medications were excluded.

The researchers included in their study 529 assessments from 164 patients. They separated patients into three groups based on their last MoCA score—those who developed dementia (33 patients), those who returned to normal cognition (48 patients), and those who maintained MoCA scores in the MCI range (83 patients). In a model that predicted future MoCA score categories with 78% accuracy, the most important subscores were visuospatial, attention, language, and orientation, “but, interestingly, not delayed recall,” Dr. Mackenzie and colleagues said.

“A prevailing theory of cognitive decline in Parkinson’s disease postulates that visuospatial ‘posterior-cortical’ impairments are due to Lewy body deposition, whereas frontal executive dysfunction reflects ‘on–off’ state,” the researchers said. “Interestingly, language scores and memory function in delayed recall were the items that improved the most” in patients who reverted from MCI to normal cognition. “Whether the best approach to assess risk of conversion to dementia is to focus exclusively on these MoCA sections, or alternatively, employing multiple tests that target these cognitive domains, remains to be seen,” the researchers concluded. Patients with Parkinson’s disease–associated MCI at any time “should likely be followed more closely for cognitive decline, as they seem to be at increased risk for developing dementia, even if there is interval maintenance of MCI or return to normal cognition.”

—Jake Remaly

Despite days of intense negotiations and last-minute concessions to win over wavering GOP conservatives and moderates, House Republican leaders Friday failed to secure enough support to pass their plan to repeal and replace the Affordable Care Act.

House Speaker Paul Ryan pulled the bill from consideration after he rushed to the White House to tell President Donald Trump that there weren’t the 216 votes necessary for passage.

“We came really close today, but we came up short,” he told reporters at a hastily called news conference.

When pressed about what happens to the federal health law, he added, “Obamacare is the law of the land. … We’re going to be living with Obamacare for the foreseeable future.”

President Trump laid the blame at the feet of Democrats, complaining that not one was willing to help Republicans on the measure, and he warned again that the Obamacare insurance markets are in serious danger. “Bad things are going to happen to Obamacare,” he told reporters at the White House. “There’s not much you can do to help it. I’ve been saying that for a year and a half. I said, look, eventually, it’s not sustainable. The insurance companies are leaving.”

But he said the collapse of the bill might allow Republicans and Democrats to work on a replacement. “I honestly believe the Democrats will come to us and say, ‘Look, let’s get together and get a great health care bill or plan that’s really great for the people of our country,’” he said.

Mr. Ryan originally had hoped to hold a floor vote on the measure Thursday – timed to coincide with the 7th anniversary of the ACA – but decided to delay that effort because GOP leaders didn’t have enough “yes” votes. The House was in session Friday, before his announcement, while members debated the bill.

House Democratic leader Nancy Pelosi (Calif.) said the speaker’s decision to pull the bill “is pretty exciting for us … a victory for the Affordable Care Act, more importantly for the American people.”

The legislation was damaged by a variety of issues raised by competing factions of the party. Many members were nervous about reports by the Congressional Budget Office showing that the bill would lead eventually to 24 million people losing insurance, while some moderate Republicans worried that ending the ACA’s Medicaid expansion would hurt low-income Americans.

At the same time, conservatives, especially the hard-right House Freedom Caucus that often has needled party leaders, complained that the bill kept too much of the ACA structure in place. They wanted a straight repeal of Obamacare, but party leaders said that couldn’t pass the Senate, where Republicans don’t have enough votes to stop a filibuster. They were hoping to use a complicated legislative strategy called budget reconciliation that would allow them to repeal parts of the ACA that only affect federal spending.

The decision came after a chaotic week of negotiations, as party leaders sought to woo more conservatives. The president lobbied 120 members through personal meetings or phone calls, according to a count provided Friday by his spokesman, Sean Spicer. “The president and the team here have left everything on the field,” Mr. Spicer said.

On Thursday evening, Mr. Trump dispatched Office of Management and Budget Director Mick Mulvaney to tell his former House GOP colleagues that the president wanted a vote on Friday. It was time to move on to other priorities, including tax reform, he told House Republicans.

“He said the president needs this, the president has said he wants a vote tomorrow, up or down. If for any reason it goes down, we’re just going to move forward with additional parts of his agenda. This is our moment in time,” Rep. Chris Collins (R-N.Y.), a loyal Trump ally, told reporters late Thursday. “If it doesn’t pass, we’re moving beyond health care. … We are done negotiating.”

Trump’s edict clearly irked some lawmakers, including the Freedom Caucus chairman, Rep. Mark Meadows (R-N.C), whose group of more than two dozen members represented the strongest bloc against the measure.

“Anytime you don’t have 216 votes, negotiations are not totally over,” he told reporters who had surrounded him in a Capitol basement hallway as he headed in to the party’s caucus meeting.

President Trump, Speaker Ryan, and other GOP lawmakers tweaked their initial package in a variety of ways to win over both conservatives and moderates. But every time one change was made to win votes in one camp, it repelled support in another.

The White House on Thursday accepted conservatives’ demands that the legislation strip federal guarantees of essential health benefits from insurance policies. But that was another problem for moderates, and Democrats suggested the provision would not survive in the Senate.

Republican moderates in the House – as well as the Senate – objected to the bill’s provisions that would shift Medicaid from an open-ended entitlement to a set amount of funding for states that also would give governors and state lawmakers more flexibility over the program. Moderates also were concerned that the package’s tax credits would not be generous enough to help older Americans – who could be charged five times more for coverage than would their younger counterparts – afford coverage.

The House package also lost the support of key GOP allies, including the Club for Growth and Heritage Action. Physician, patient and hospital groups also opposed it.

But Mr. Ryan’s comments made clear how difficult this decision was. “This is a disappointing day for us,” he said. “Doing big things is hard. All of us. All of us – myself included – we will need time to reflect on how we got to this moment, what we could have done to do it better.”
 

Kaiser Health News is a national health policy news service that is part of the nonpartisan Henry J. Kaiser Family Foundation.

Despite days of intense negotiations and last-minute concessions to win over wavering GOP conservatives and moderates, House Republican leaders Friday failed to secure enough support to pass their plan to repeal and replace the Affordable Care Act.

House Speaker Paul Ryan pulled the bill from consideration after he rushed to the White House to tell President Donald Trump that there weren’t the 216 votes necessary for passage.

“We came really close today, but we came up short,” he told reporters at a hastily called news conference.

When pressed about what happens to the federal health law, he added, “Obamacare is the law of the land. … We’re going to be living with Obamacare for the foreseeable future.”

President Trump laid the blame at the feet of Democrats, complaining that not one was willing to help Republicans on the measure, and he warned again that the Obamacare insurance markets are in serious danger. “Bad things are going to happen to Obamacare,” he told reporters at the White House. “There’s not much you can do to help it. I’ve been saying that for a year and a half. I said, look, eventually, it’s not sustainable. The insurance companies are leaving.”

But he said the collapse of the bill might allow Republicans and Democrats to work on a replacement. “I honestly believe the Democrats will come to us and say, ‘Look, let’s get together and get a great health care bill or plan that’s really great for the people of our country,’” he said.

Mr. Ryan originally had hoped to hold a floor vote on the measure Thursday – timed to coincide with the 7th anniversary of the ACA – but decided to delay that effort because GOP leaders didn’t have enough “yes” votes. The House was in session Friday, before his announcement, while members debated the bill.

House Democratic leader Nancy Pelosi (Calif.) said the speaker’s decision to pull the bill “is pretty exciting for us … a victory for the Affordable Care Act, more importantly for the American people.”

The legislation was damaged by a variety of issues raised by competing factions of the party. Many members were nervous about reports by the Congressional Budget Office showing that the bill would lead eventually to 24 million people losing insurance, while some moderate Republicans worried that ending the ACA’s Medicaid expansion would hurt low-income Americans.

At the same time, conservatives, especially the hard-right House Freedom Caucus that often has needled party leaders, complained that the bill kept too much of the ACA structure in place. They wanted a straight repeal of Obamacare, but party leaders said that couldn’t pass the Senate, where Republicans don’t have enough votes to stop a filibuster. They were hoping to use a complicated legislative strategy called budget reconciliation that would allow them to repeal parts of the ACA that only affect federal spending.

The decision came after a chaotic week of negotiations, as party leaders sought to woo more conservatives. The president lobbied 120 members through personal meetings or phone calls, according to a count provided Friday by his spokesman, Sean Spicer. “The president and the team here have left everything on the field,” Mr. Spicer said.

On Thursday evening, Mr. Trump dispatched Office of Management and Budget Director Mick Mulvaney to tell his former House GOP colleagues that the president wanted a vote on Friday. It was time to move on to other priorities, including tax reform, he told House Republicans.

“He said the president needs this, the president has said he wants a vote tomorrow, up or down. If for any reason it goes down, we’re just going to move forward with additional parts of his agenda. This is our moment in time,” Rep. Chris Collins (R-N.Y.), a loyal Trump ally, told reporters late Thursday. “If it doesn’t pass, we’re moving beyond health care. … We are done negotiating.”

Trump’s edict clearly irked some lawmakers, including the Freedom Caucus chairman, Rep. Mark Meadows (R-N.C), whose group of more than two dozen members represented the strongest bloc against the measure.

“Anytime you don’t have 216 votes, negotiations are not totally over,” he told reporters who had surrounded him in a Capitol basement hallway as he headed in to the party’s caucus meeting.

President Trump, Speaker Ryan, and other GOP lawmakers tweaked their initial package in a variety of ways to win over both conservatives and moderates. But every time one change was made to win votes in one camp, it repelled support in another.

The White House on Thursday accepted conservatives’ demands that the legislation strip federal guarantees of essential health benefits from insurance policies. But that was another problem for moderates, and Democrats suggested the provision would not survive in the Senate.

Republican moderates in the House – as well as the Senate – objected to the bill’s provisions that would shift Medicaid from an open-ended entitlement to a set amount of funding for states that also would give governors and state lawmakers more flexibility over the program. Moderates also were concerned that the package’s tax credits would not be generous enough to help older Americans – who could be charged five times more for coverage than would their younger counterparts – afford coverage.

The House package also lost the support of key GOP allies, including the Club for Growth and Heritage Action. Physician, patient and hospital groups also opposed it.

But Mr. Ryan’s comments made clear how difficult this decision was. “This is a disappointing day for us,” he said. “Doing big things is hard. All of us. All of us – myself included – we will need time to reflect on how we got to this moment, what we could have done to do it better.”
 

Kaiser Health News is a national health policy news service that is part of the nonpartisan Henry J. Kaiser Family Foundation.

Despite days of intense negotiations and last-minute concessions to win over wavering GOP conservatives and moderates, House Republican leaders Friday failed to secure enough support to pass their plan to repeal and replace the Affordable Care Act.

House Speaker Paul Ryan pulled the bill from consideration after he rushed to the White House to tell President Donald Trump that there weren’t the 216 votes necessary for passage.

“We came really close today, but we came up short,” he told reporters at a hastily called news conference.

When pressed about what happens to the federal health law, he added, “Obamacare is the law of the land. … We’re going to be living with Obamacare for the foreseeable future.”

President Trump laid the blame at the feet of Democrats, complaining that not one was willing to help Republicans on the measure, and he warned again that the Obamacare insurance markets are in serious danger. “Bad things are going to happen to Obamacare,” he told reporters at the White House. “There’s not much you can do to help it. I’ve been saying that for a year and a half. I said, look, eventually, it’s not sustainable. The insurance companies are leaving.”

But he said the collapse of the bill might allow Republicans and Democrats to work on a replacement. “I honestly believe the Democrats will come to us and say, ‘Look, let’s get together and get a great health care bill or plan that’s really great for the people of our country,’” he said.

Mr. Ryan originally had hoped to hold a floor vote on the measure Thursday – timed to coincide with the 7th anniversary of the ACA – but decided to delay that effort because GOP leaders didn’t have enough “yes” votes. The House was in session Friday, before his announcement, while members debated the bill.

House Democratic leader Nancy Pelosi (Calif.) said the speaker’s decision to pull the bill “is pretty exciting for us … a victory for the Affordable Care Act, more importantly for the American people.”

The legislation was damaged by a variety of issues raised by competing factions of the party. Many members were nervous about reports by the Congressional Budget Office showing that the bill would lead eventually to 24 million people losing insurance, while some moderate Republicans worried that ending the ACA’s Medicaid expansion would hurt low-income Americans.

At the same time, conservatives, especially the hard-right House Freedom Caucus that often has needled party leaders, complained that the bill kept too much of the ACA structure in place. They wanted a straight repeal of Obamacare, but party leaders said that couldn’t pass the Senate, where Republicans don’t have enough votes to stop a filibuster. They were hoping to use a complicated legislative strategy called budget reconciliation that would allow them to repeal parts of the ACA that only affect federal spending.

The decision came after a chaotic week of negotiations, as party leaders sought to woo more conservatives. The president lobbied 120 members through personal meetings or phone calls, according to a count provided Friday by his spokesman, Sean Spicer. “The president and the team here have left everything on the field,” Mr. Spicer said.

On Thursday evening, Mr. Trump dispatched Office of Management and Budget Director Mick Mulvaney to tell his former House GOP colleagues that the president wanted a vote on Friday. It was time to move on to other priorities, including tax reform, he told House Republicans.

“He said the president needs this, the president has said he wants a vote tomorrow, up or down. If for any reason it goes down, we’re just going to move forward with additional parts of his agenda. This is our moment in time,” Rep. Chris Collins (R-N.Y.), a loyal Trump ally, told reporters late Thursday. “If it doesn’t pass, we’re moving beyond health care. … We are done negotiating.”

Trump’s edict clearly irked some lawmakers, including the Freedom Caucus chairman, Rep. Mark Meadows (R-N.C), whose group of more than two dozen members represented the strongest bloc against the measure.

“Anytime you don’t have 216 votes, negotiations are not totally over,” he told reporters who had surrounded him in a Capitol basement hallway as he headed in to the party’s caucus meeting.

President Trump, Speaker Ryan, and other GOP lawmakers tweaked their initial package in a variety of ways to win over both conservatives and moderates. But every time one change was made to win votes in one camp, it repelled support in another.

The White House on Thursday accepted conservatives’ demands that the legislation strip federal guarantees of essential health benefits from insurance policies. But that was another problem for moderates, and Democrats suggested the provision would not survive in the Senate.

Republican moderates in the House – as well as the Senate – objected to the bill’s provisions that would shift Medicaid from an open-ended entitlement to a set amount of funding for states that also would give governors and state lawmakers more flexibility over the program. Moderates also were concerned that the package’s tax credits would not be generous enough to help older Americans – who could be charged five times more for coverage than would their younger counterparts – afford coverage.

The House package also lost the support of key GOP allies, including the Club for Growth and Heritage Action. Physician, patient and hospital groups also opposed it.

But Mr. Ryan’s comments made clear how difficult this decision was. “This is a disappointing day for us,” he said. “Doing big things is hard. All of us. All of us – myself included – we will need time to reflect on how we got to this moment, what we could have done to do it better.”
 

Kaiser Health News is a national health policy news service that is part of the nonpartisan Henry J. Kaiser Family Foundation.

Influenza activity took another healthy step down as outpatient visits continued to drop, according to the Centers for Disease Control and Prevention.

The proportion of outpatient visits for influenza-like illness (ILI) was down to 3.2% for the week ending March 18, 2017, the CDC reported, compared with 3.6% the week before. (The figure of 3.7% previously reported for last week has been adjusted this week, so the halt in the decline in outpatient visits was actually more of a slowdown.) The national baseline for outpatient ILI visits is 2.2%.

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Influenza activity took another healthy step down as outpatient visits continued to drop, according to the Centers for Disease Control and Prevention.

The proportion of outpatient visits for influenza-like illness (ILI) was down to 3.2% for the week ending March 18, 2017, the CDC reported, compared with 3.6% the week before. (The figure of 3.7% previously reported for last week has been adjusted this week, so the halt in the decline in outpatient visits was actually more of a slowdown.) The national baseline for outpatient ILI visits is 2.2%.

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Influenza activity took another healthy step down as outpatient visits continued to drop, according to the Centers for Disease Control and Prevention.

The proportion of outpatient visits for influenza-like illness (ILI) was down to 3.2% for the week ending March 18, 2017, the CDC reported, compared with 3.6% the week before. (The figure of 3.7% previously reported for last week has been adjusted this week, so the halt in the decline in outpatient visits was actually more of a slowdown.) The national baseline for outpatient ILI visits is 2.2%.

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MELBOURNE – SPECT imaging can identify abnormalities in brain perfusion in patients with multiple antiphospholipid antibodies and neuropsychiatric symptoms, but without a history of thrombosis, according to a study presented at an international congress on systemic lupus erythematosus.

The retrospective study by researchers from National Taiwan University Hospital addresses the challenge posed by patients who have antiphospholipid antibodies and neuropsychiatric symptoms but do not meet the full criteria for antiphospholipid syndrome because of a lack of a history of thromboembolism. Current antiphospholipid syndrome classification criteria are based on thrombosis or pregnancy loss, with a third category of noncriteria manifestations that include a range of neuropsychiatric symptoms, said presenter Ting-Syuan Lin, MD, of the Yun-Lin Branch of National Taiwan University Hospital.

MELBOURNE – SPECT imaging can identify abnormalities in brain perfusion in patients with multiple antiphospholipid antibodies and neuropsychiatric symptoms, but without a history of thrombosis, according to a study presented at an international congress on systemic lupus erythematosus.

The retrospective study by researchers from National Taiwan University Hospital addresses the challenge posed by patients who have antiphospholipid antibodies and neuropsychiatric symptoms but do not meet the full criteria for antiphospholipid syndrome because of a lack of a history of thromboembolism. Current antiphospholipid syndrome classification criteria are based on thrombosis or pregnancy loss, with a third category of noncriteria manifestations that include a range of neuropsychiatric symptoms, said presenter Ting-Syuan Lin, MD, of the Yun-Lin Branch of National Taiwan University Hospital.

MELBOURNE – SPECT imaging can identify abnormalities in brain perfusion in patients with multiple antiphospholipid antibodies and neuropsychiatric symptoms, but without a history of thrombosis, according to a study presented at an international congress on systemic lupus erythematosus.

The retrospective study by researchers from National Taiwan University Hospital addresses the challenge posed by patients who have antiphospholipid antibodies and neuropsychiatric symptoms but do not meet the full criteria for antiphospholipid syndrome because of a lack of a history of thromboembolism. Current antiphospholipid syndrome classification criteria are based on thrombosis or pregnancy loss, with a third category of noncriteria manifestations that include a range of neuropsychiatric symptoms, said presenter Ting-Syuan Lin, MD, of the Yun-Lin Branch of National Taiwan University Hospital.